Pulmonary and Critical Care Medicine (S-111-PULM), VA Puget Sound Health Care System, 1660 South Columbian Way, Seattle, WA 98108, USA.
Respir Physiol Neurobiol. 2013 Mar 1;186(1):33-9. doi: 10.1016/j.resp.2012.12.014. Epub 2013 Jan 7.
Evidence from liquid-filled rat lungs supported the presence of CO2-dependent, active relaxation of parenchyma under normoxia by unknown mechanisms (Emery et al., 2007). This response may improve matching of alveolar ventilation (V˙A) to perfusion (Q˙) by increasing compliance and V˙A in overperfused (high CO2) regions, and decrease V˙A in underperfused regions. Here, we have more directly studied CO2-dependent parenchymal relaxation and tested a hypothesized role for actin-myosin interaction in this effect. Lung parenchymal strips (∼1.5mm×1.5mm×15mm) from 16 rats were alternately exposed to normoxic hypocapnia ( [Formula: see text] ) or hypercapnia ( [Formula: see text] ). Seven specimens were used to construct length-tension curves, and nine were tested with and without the myosin blocker 2,3-butanedione monoxime (BDM). The results demonstrate substantial, reversible CO2-dependent changes in parenchyma strip recoil (up to 23%) and BDM eliminates this effect, supporting a potentially important role for parenchymal myosin in V˙A/Q˙ matching.
来自充满液体的大鼠肺的证据支持在正常氧合条件下通过未知机制存在 CO2 依赖性、实质的主动弛豫(Emery 等人,2007 年)。这种反应可以通过增加顺应性和过度灌注(高 CO2)区域的 V˙A 来改善肺泡通气(V˙A)与灌注(Q˙)的匹配,并减少灌注不足区域的 V˙A。在这里,我们更直接地研究了 CO2 依赖性实质弛豫,并测试了肌动球蛋白相互作用在这种效应中的假设作用。来自 16 只大鼠的肺实质条(约 1.5mm×1.5mm×15mm)交替暴露于低氧性低碳酸血症([Formula: see text])或高碳酸血症([Formula: see text])下。七个标本用于构建长度-张力曲线,九个标本在有和没有肌球蛋白抑制剂 2,3-丁二酮单肟(BDM)的情况下进行测试。结果表明实质条回弹中存在大量、可逆转的 CO2 依赖性变化(高达 23%),BDM 消除了这种效应,支持实质肌球蛋白在 V˙A/Q˙匹配中具有潜在的重要作用。